IPH/IVH

FACTS

Usually hypertensive, get ready for an EVD if mental status poor
Etiologies:
Most common
  • Hypertensive (most common) usually in basal ganglia, thalamus, pons, cerebellum
  • Amyloid bleeds (lobar)
Less common
  • arteriovenous malformation (anywhere but usually superficial/lobar)
  • neoplasms, most commonly metastatic melanona, choriocarcinoma, oligodendroglioma, any glioma
  • venous thrombosis (parasagittal)
  • blood dyscrasias/fat emboli (scattered petechial)

HPI

  • What was systolic blood pressure on arrival?
  • Medical history
    • AC/AP use
    • Known HTN? adherent to home meds?
    • Prior MI / stroke
    • smoker
    • amyloid angiopathy or bleeding diathesis in patient or family
    • any cancer history
    • dementia (check meds)
  • Social history
    • cocaine/amphetamine user
  • Review of systems
    • did the patient seize
    • Hydro symptoms:
      • drowsy / vomiting

PHYSICAL EXAM

mental status is most important. Calculate GCS for the ICH score

IMAGING

CTH non-contrast
CTA H&N
MRI Brain w/o can show multiple amyloid bleeds not seen on dry CT
Locations of hypertensive bleeds
  • basal ganglia (putamen) (60%)
  • thalamus (20%)
  • pons (10%)
  • cerebellum (10%)
A/P
Admit to neuro-ICU (stroke if no EVD, NSGY if EVD)
Stroke consult
Reverse AP/AC
EVD pending mental status, no official scale but can basically use hunt hess, will be attending dependent
CAP 140
HOB > 30
Keppra usually only if seized (no prophylactic unless blood burden massive)
6 hour dry stability scan (make sure dual energy if received contrast)
MRI Brain w/wo to rule out lesion, this is not a priority and should only be done once stability of bleed established on ≥ 6 hr dry CT and if patient is stable enough for transport / lying flat for 20-30 minutes
+/- DSA (can also be an AVM)

Amyloid Bleeds

Figure 1: Lobar Amyloid Bleed
Figure 1: Lobar Amyloid Bleed
Figure 2: Hypertensive bi-hemispheric IPH. This was such a profound bleed with origin of bleed difficult to determine however patient was SBP to 200s at time of presentation.
Figure 2: Hypertensive bi-hemispheric IPH. This was such a profound bleed with origin of bleed difficult to determine however patient was SBP to 200s at time of presentation.
Figure 3: Hypertensive RIGHT thalamic bleed with significant intraventricular extension, ventriculomegaly, and hydrocephalus.
Figure 3: Hypertensive RIGHT thalamic bleed with significant intraventricular extension, ventriculomegaly, and hydrocephalus.
Figure 4: Pontine hemorrhage
Figure 4: Pontine hemorrhage